An 80-something tripped and sustained a hip fracture.
The patient had no cardiac symptoms, no syncope, no CP or SOB. He was perfectly fine.
He had a 12-lead ECG in the ED as part of screening:
You know there is something wrong at least partly because it is on this blog.
But this was looked at in a cursory fashion by a couple very busy emergency physicians and no serious abnormality was noticed.
First note that the QRS complexes are grouped. Then you can see that there are P-waves which did not conduct (#'s 3 and 8). There is no PR lengthening prior to the blocked conduction; therefore, it is not Mobitz I (Wenckebach), which would be a benign AV block, but rather Mobitz II.
They did not see that this is 2nd degree AV block Mobitz II. When I saw it I immediately recognized it, after which it was clear to the providers.
Mobitz II has dropped beats without any prior PR lengthening, and is at risk of progressing to 3rd degree (complete) AV block. Mobitz II is often below the AV node and therefore often does not respond to atropine. When the QRS is wide, then it is much more likely to represent blockade below the AV node, and is more likely to be dangerous.
In this case, there is also RBBB with LAFB, which suggests block below the bundle of His.
Clinical Course
Pacer pads were placed on his chest and he was admitted to the ICU with cardiology and EP consultation.
Had he had this rhythm associated with symptoms such as syncope, or associated with acute MI, then he would undergo immediate transvenous pacer placement.
He was kept overnight on telemetry and on the cardiac monitor he was noted to have intermittent bradycardia. Some of them were during sleep hours, however there was another episode around 10 PM where it is not very clear whether he was asleep or not.
Of note, the PR interval is normal during the conducted beats. This is important because it suggests that vagal tone did not have anything to do with the AV block, and suggests a more pernicious etiology.
There was concern that, during hip surgery, he would develop complete AV block.
A temporary pacer was placed.
An EP study to assess need for permanent pacer was undertaken and showed no convincing evidence of Infra-His block. No permanent pacer was placed.
Learning Point:
Assess the ECG systematically or you will miss something, especially when it is a screening ECG (i. e., the patient does not have cardiac symptoms)!
These are the characteristics of a normal ECG.
Note that you must assess the rate, rhythm, P-waves, PR interval, and a QRS for every P-wave as part of a systematic approach.
The patient had no cardiac symptoms, no syncope, no CP or SOB. He was perfectly fine.
He had a 12-lead ECG in the ED as part of screening:
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| Interpretation? |
You know there is something wrong at least partly because it is on this blog.
But this was looked at in a cursory fashion by a couple very busy emergency physicians and no serious abnormality was noticed.
First note that the QRS complexes are grouped. Then you can see that there are P-waves which did not conduct (#'s 3 and 8). There is no PR lengthening prior to the blocked conduction; therefore, it is not Mobitz I (Wenckebach), which would be a benign AV block, but rather Mobitz II.
They did not see that this is 2nd degree AV block Mobitz II. When I saw it I immediately recognized it, after which it was clear to the providers.
Mobitz II has dropped beats without any prior PR lengthening, and is at risk of progressing to 3rd degree (complete) AV block. Mobitz II is often below the AV node and therefore often does not respond to atropine. When the QRS is wide, then it is much more likely to represent blockade below the AV node, and is more likely to be dangerous.
In this case, there is also RBBB with LAFB, which suggests block below the bundle of His.
Clinical Course
Pacer pads were placed on his chest and he was admitted to the ICU with cardiology and EP consultation.
Had he had this rhythm associated with symptoms such as syncope, or associated with acute MI, then he would undergo immediate transvenous pacer placement.
He was kept overnight on telemetry and on the cardiac monitor he was noted to have intermittent bradycardia. Some of them were during sleep hours, however there was another episode around 10 PM where it is not very clear whether he was asleep or not.
Of note, the PR interval is normal during the conducted beats. This is important because it suggests that vagal tone did not have anything to do with the AV block, and suggests a more pernicious etiology.
There was concern that, during hip surgery, he would develop complete AV block.
A temporary pacer was placed.
An EP study to assess need for permanent pacer was undertaken and showed no convincing evidence of Infra-His block. No permanent pacer was placed.
Learning Point:
Assess the ECG systematically or you will miss something, especially when it is a screening ECG (i. e., the patient does not have cardiac symptoms)!
These are the characteristics of a normal ECG.
Note that you must assess the rate, rhythm, P-waves, PR interval, and a QRS for every P-wave as part of a systematic approach.
NSR,
normal rate
Upright
P wave in lead II
Biphasic P wave in V1
PR
interval 120 – 200 msec
QRS for every P-wave, same PR interval
QRS less than 110 msec
Normal QRS Axis (-30 to 90 degrees)
Voltage
normal
Normal
septal Q waves
Normal
R-wave progression
Normal
ST segments
Normal T-wave size
Normal
T wave axis
Normal
QT
Normal
U-waves
===================================
MY Comment by KEN GRAUER, MD (1/1/2020):
===================================
I like nothing better than a good arrhythmia to start of the new decade! So our THANKS to Dr. Smith for doing just that. I’d add the following thoughts to the excellent discussion by Dr. Smith.
- As per Dr. Smith — perhaps the KEY Learning Point is the need to use a Systematic Approach to ECG Interpretation (and especially to rhythm interpretation). Readers of Dr. Smith’s blog know I constantly emphasize this point (See My Comment in the June 28, 2019 post on Dr. Smith’s blog).
- CLICK HERE — For “My Take” on Systematic 12-Lead interpretation.
- CLICK HERE — For “My Take” on Systematic Rhythm interpretation.
Regarding this 12-lead ECG + Rhythm Strip:
- As per Dr. Smith — There is underlying RBBB/LAHB — but there are no acute changes.
- Regarding the rhythm — we look first at the long lead rhythm strip. The underlying rhythm is sinus (ie, upright P wave in lead II) — with slight sinus arrhythmia (slight variation in the R-R interval).
- The QRS complex is wide (as above = RBBB/LAHB).
- The overall R-R interval is fairly regular — but there are 2 pauses on this lead II rhythm strip.
- As per Dr. Smith — the PR interval remains constant for the conducted beats throughout this rhythm strip! PEARL #1 — The KEY to diagnosing Mobitz II, 2nd-Degree AV Block — is that you see consecutively conducted beats, in which the PR interval does not increase. The reason you cannot distinguish with certainty between Mobitz I vs Mobitz II forms of 2nd-Degree AV Block when there is strict 2:1 AV conduction — is that you never get to see 2 conducted beats in a row when there is 2:1 AV block (which means that you can not tell for sure if the PR interval would increase [as in Mobitz I ] IF it had a chance to do so).
- The patient in this case was in his 80s. We have no idea for how long he has lived with bifascicular block + Mobitz II. This AV block could be recent or acute (therefore the rationale for placement of a temporary pacemaker) — but given the subsequent negative EP study — the thought was that permanent pacing was probably not necessary at this point in time (and might never be necessary for this patient in his 80s).
- That said — this potentially serious (life-threatening) form of AV block should not have been overlooked by the initial providers. PEARL #2 — IF emergency providers would begin to routinely carry and use a pair of Calipers — they will doubtlessly surprise themselves by increasing their speed for interpreting complex arrhythmias — and, I bet they will never again miss another case of AV block!
- PEARL #3 — Assuming this 80-something patient maintains his satisfactorily functional lifestyle status — I would recheck a 24-hour Holter monitor on him fairly soon (and perhaps periodically as an outpatient in the future) — to ensure that prolonged bradycardia does not subsequently develop (ie, Despite benign overnight monitoring on telemetry — there still is significant potential risk for subsequent development of prolonged bradycardia).
- If you click on SHOW MORE (under the video on the YouTube page) — You’ll find a detailed timed/linked Contents of all in this video.
- CLICK HERE — to go directly to the part (beginning at 30:09) that deals with the 3 types of 2nd-Degree AV Block.
P.S. (1/2/2020): Since there have been some questions regarding atrial activity in this case (P waves are of low amplitude) — I am adding Figure-1, in which I have numbered the beats and labeled P waves.
- Calipers greatly facilitate establishing that P waves are quite regular here (perhaps with slight variation in some P-P interval).
- Calipers also verify that the PR interval is not increasing (ie, this is not Mobitz I ).
- PEARL: The best (easiest) way to tell if the PR interval during a sequence of beats is increasing — is to look at the PR interval just before the pause (ie, the PR interval before beat #2) — and compare this to the PR interval at the end of the pause (ie, the PR interval before beat #3). Do this for each pause in the tracing (ie, Compare the PR interval before beat #6 with the PR interval before beat #7). Note that there is NO difference between any of these PR intervals — thus, the PR interval remains constant throughout, and this is Mobitz II.
- The PR interval is not prolonged. The easiest way to measure the PR interval is to find a P wave on the rhythm strip that begins on a heavy line (BLUE arrow in Figure-1). Note that the QRS complex of beat #2 begins slightly before the next heavy line — which means that the PR interval is definitely not more than 1 large box in duration. This is a normal PR interval (Given the wide range of "normal" PR intervals — my preference is not to call 1st-Degree AV Block until the PR interval is at least 0.22 second in duration).
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| Figure-1: The ECG in this case (See text). |
Thanks for a nice case!
ReplyDeleteI would additionaly say "trifascicular block" describing this ECG - kind of traditional to my local health care providers.
@ Max Romanchenko — THANK YOU for your comment. I have just now added (after your sent in your comment) a “P.S.” to what I wrote yesterday, together with a labeled Figure-1 for the tracing in this case. FIRST — as per the BLUE arrow in the long lead rhythm strip (and my explanation in the P.S.) — the PR interval in this tracing is not prolonged. SECOND — Even if the PR interval was prolonged, the term, “tri-fascicular block” is no longer in favor. The reason is that despite RBBB + LAHB + 1st degree av block — we are simply UNABLE from the surface ECG to know IF the “site” of the 1st degree av block is before the His (ie, in the atria or AV node) — or lower down in the left posterior hemifascicle. Current recommendations therefore favor simply describing the conduction defects you identify WITHOUT use of the imprecise term “trifascicular block” — :)
DeleteBeautiful case to start the year! Thanks!!
ReplyDelete@ Docd91 — THANK YOU! — :)
DeleteHi....Can u explain why it is not Non-Conducted APC ? Please
ReplyDeleteThe KEY to diagnosing an AV block — is to recognize that there is an underlying regular (or almost regular) sinus rhythm. RED arrows in my Figure-1 (above) show regular-occurring P waves. For this to be a "blocked ( = non-conducted) PAC", you would have to identify an EARLY-occurring P wave. Typically, non-conducted PACs occur VERY early in the cycle — and this is clearly not what is happening here — :)
DeleteAccording to the AHA-ACC 2018, there is indication of PPM in case of AV Block Mobitz 2 regardless of symptom. But this patient was not implanted. So, what do you think about this case Prof. Ken Grauer.
ReplyDeleteTHANKS for your comment Nguyen! I agree with you — but I "wasn't there", and I don't know details regarding this case. It sounds like this WAS a very "functional" 80-something year old (but these details about "quality-of-life" that are so individual and difficult to assess "on paper" are largely unknown). We also do not know HOW SLOW the "intermittent bradycardia" that was reported got to ... For these reasons, I emphasized in My Comment the need to repeat the 24-hour Holter SOON, and then perhaps periodically (In my experience, despite the "best" of telemetry technicians — sometimes significant arrhythmias may be missed on tele that ARE found on Holter). All that said — EP Cardiology DID evaluate this patient — so we have to trust their final judgment. But it WOULD be interesting to know more details about the decisions made in this case! THANKS again for your thoughts! — :)
DeleteYes, thank you very much, sir!
Deleteexcellent.
ReplyDeleteas opposed to Ken, i like to start the new year with an ARVD, or perhaps a bottle of Lown-Ganong- Levine.
yes. potentially life threatening miss, especially before surgery.
i wonder how the patient broke his hip? simple trip, or rather transient syncope secondary to his heart.
thanks Steve and Ken.
Agree completely Tom! So I would ADD your comment to the concern voiced above by Nguyen Chi Tinh ( + my reply to him) — that it would seem given Mobitz II + a fall resulting in a hip fracture (truly a "trip" — or some syncope first that caused the patient to "trip"?) + "intermittent bradycardia" on brief telemetry monitoring — that a permanent pacemaker would be indicated ... but we "weren't there" — and LACK clinical details in this case. It's GOOD to raise these questions — though unfortunately we don't have the answers in this case.
DeleteBy patient history, there was little doubt that it was a mechanical fall.
DeleteI always have doubts weather to implant a PPM to such patients. According to guidelines I should do it (Nguyen Chi Tinh, 👍), in real practice when the patient is compliant, physically active and adequately assess possible symptoms I stick to followup with regular ECG + 24h monitoring (approx every 3 months).
DeleteAnother possible solution is implanting a PPM and setting hysteresis on, so paced contractions will take only couple percent.
Is there no prior inferior M.I according the ECG ?
ReplyDelete@ G.H. — Excellent question you ask! Wish I had a simple answer … — so, “It depends”. The BEST (perhaps only) way to answer your question with certainty, would be IF you KNEW this patient — and you KNEW that in the past the patient had an inferior MI. Unfortunately, that information is not available to us. From an ECG standpoint — there are similarities in the way I will answer you with what I just wrote in answer to the questions by Unknown (See below) — in that there are “competing conditions”. So, with Inf. MI that generates inferior Q waves — the initial depolarization vector moves AWAY from the inferior leads = it moves superiorly (this superior movement is what generates inferior Q waves). In contrast, with LAHB — initial depolarization moves inferiorly and toward the right. Because of these “competing” (ie, opposing) vector forces — one condition may mask the other on ECG. This has been studied. Vector loops (which aren’t done much anymore) can often provide the answer. From the surface ECG — the KEY to determining IF there has been prior Inferior MI in a patient with LAHB (or here, in a patient with RBBB/LAHB) — is whether there is a Q wave in lead II. But there is NOT a Q in lead II in this case (instead, there is a very small-but-present initial r wave). The fact that there are QS complexes in leads III and aVF in this case is suggestive of prior Inf. MI, but not definitive. Looking further — Vector analysis suggests that when there are terminal R waves in both leads aVR and aVL — that IF the R (in this case an r’) in lead aVR occurs AFTER the R in lead aVL — that there is LAHB (because this implies that terminal depol is moving superiorly) — and although the r’ in Figure 1 is TINY, it DOES seem to occur AFTER the R wave peak in lead aVL. BOTTOM LINE: I suspect this patient most probably has BOTH prior Inf. MI + LAHB — but lack of a Q in lead II makes it difficult to be 100% certain of this. In any event — there do not appear to be any acute ST-T wave changes. LEARNING POINT — It’s good to appreciate that the presence of “competing conditions” makes ECG diagnosis much more challenging! — :)
DeleteThanks dear prof. 😊
DeleteI did't understand why there is RBBB, because i could not see caracteristic morfhology, that is neither RSR’ pattern in V1-3 nor wide, slurred S wave in the lateral leads (I, aVL, V5-6). Futhermore, i want to know if is there LVH, because R in aVL is more than 11 mm and R in I plus S in III is more than 25 mm.
ReplyDelete@ Unknown — Ideally, one defines complete RBBB as a QRS complex of ≥0.11-0.12 second + either an rSR’ in lead V1 - OR - an “RBBB Equivalent” pattern in V1 + wide terminal S waves in lateral leads I & V6. That said — the presence of OTHER conditions may mask or otherwise alter this definition from its pure form. So scarring, prior MI, other conduction defects, chamber enlargement may ALL alter the above “pure” definition for RBBB or LBBB … The QRS complex in Figure-1 IS wide (I measure 3 little boxes in duration = 0.12 second). There IS a wide terminal S wave in lead V6 (albeit not in lead I). And we have a QR pattern in lead V1, with what looks to be a fairly wide initial Q wave. Thus, prior septal infarction may have altered QRS morphology in lead V1 here. I say “may” — because there is a lot of artifact, and morphology in V2 is less than definite. But what we DO have — is a predominant R wave in lead V1 — and there are a limited number of conditions that do this (See THIS LINK — http://ecg-interpretation.blogspot.com/2014/01/ecg-interpretation-review-81-tall-r.html — It IS well established that you can have RBBB without that classic rSR’ — IF you have a wide QRS, idealy with S wave in some lateral lead — and what I have termed a “RBBB Equivalent pattern” — and the QR we see in Figure 1 clearly fits the defintion of an “RBBB Equivalent” (Listen to the next few minutes in this ECG Video of mine — https://youtu.be/WQHzbZXcU4Y?t=620 ). As to LVH — it is probably present in this 80-something man who OBVIOUSLY has singnificant underlying heart disease (judging from his bifascicular block + Mobitz II). The problem is that we again have a “competing condition” (ie, LAHB) — and because LAHB alters the sequence of ventricular depolarization, the usual ECG criteria for diagnosing LVH are NOT as accurate. So YES, there “probably” IS LVH in Figure 1 — because the R in aVL is ≥12mm — but I’d ADD the qualifier “probably”, because the fact that there is RBBB & LAHB means that the accuracy of this voltage criteria is just NOT optimal. There IS some slowly downsloping ST depression in lead aVL that COULD be consistent with LV “strain” — but I really don’t see LV “strain” in other lateral leads. BOTTOM LINE: The presence of “competing conditions” makes precise ECG interpretation challenging, and renders interpretation into an ART which is less than perfectly accurate. NICE discussion! — :)
DeleteDoes this patient have:
ReplyDeleteleft atrial enlargement (notched p waves in lead II)?
left ventricle hypertrophy(based on AVL lead)?
Poor R wave progression?
pathologic Q waves in lead III & AVF & V1 showing old inferior MI?
@ Aidin. EXCELLENT Questions you ask! Here are my Answers: #1) I would not call LAA (left atrial enlargement). It’s BEST in my opinion to UNDERCALL atrial enlargement on ECG — because of poor sensitivity and specificity of the ECG for this purpose. Much of the time, notched P waves actually indicate intra-atrial conduction defects rather than true atrial “enlargement”. In this particular case — there is too much artifact, the notch in lead II is present but barely — and the P wave is really not prolonged. I wouldn’t call LAA ( = my opinion — which I amplify here = http://ecg-interpretation.blogspot.com/2013/09/ecg-interpretation-review-75-chamber.html ). #2) YES — There IS suggestion of LVH based on R in aVL ≥12mm + the ST sagging in aVL is what I’d call a “strain equivalent” (for more on this see here = http://ecg-interpretation.blogspot.com/2013/08/ecg-interpretation-review-73-lvh.html ) — #3) The term “poor R wave progression” is not relevant in this tracing in which there is RBBB — #4) Diagnosis of prior MI is often much more difficult in association with underlying LAHB, as we have here. That said — YES, the QS in leads III and aVF suggest prior Inferior MI in addition to LAHB (note that there IS a small r wave in lead II!) — and YES, the Q is quite wide in lead V1, so this DOES suggest prior septal infarction. THANKS for your interest! — :)
Delete